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Cell. 2007 Oct 5;131(1):33-45.

Communicable ulcerative colitis induced by T-bet deficiency in the innate immune system.

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  • 1Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.

Abstract

Inflammatory bowel disease (IBD) has been attributed to overexuberant host immunity or the emergence of harmful intestinal flora. The transcription factor T-bet orchestrates inflammatory genetic programs in both adaptive and innate immunity. We describe a profound and unexpected function for T-bet in influencing the behavior of host inflammatory activity and commensal bacteria. T-bet deficiency in the innate immune system results in spontaneous and communicable ulcerative colitis in the absence of adaptive immunity and increased susceptibility to colitis in immunologically intact hosts. T-bet controls the response of the mucosal immune system to commensal bacteria by regulating TNF-alpha production in colonic dendritic cells, critical for colonic epithelial barrier maintenance. Loss of T-bet influences bacterial populations to become colitogenic, and this colitis is communicable to genetically intact hosts. These findings reveal a novel function for T-bet as a peacekeeper of host-commensal relationships and provide new perspectives on the pathophysiology of IBD.

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PMID:
17923086
[PubMed - indexed for MEDLINE]
PMCID:
PMC2169385
Free PMC Article

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